The primary objective of this work is to elucidate the cellular and synaptic mechanisms responsible for the genesis of spontaneous rhythmic activity in the developing spinal cord. Experiments are performed on isolated preparations of the chick and mouse spinal cords maintained in vitro. We use electrophysiological, optical and anatomical methods to analyze the function and properties of the developing networks. Recently we have formulated a qualitative model to account for the genesis of rhythmic activity by developing spinal networks. Crucial to this model are our recent observations that network activity and synaptic transmission are depressed after a spontaneous episode. This depression arises in part because of a decrease in the responsiveness of postsynaptic glutamate and GABA receptors in part due to ionic redistribution during an episode. In isolated neonatal mice cords it has been possible to activate locomotor networks using dorsal root stimulation or bath-applied drugs. Once active, this network drives contralateral motoneurons to discharge in an alternating manner. Studies are currently in progress to identify the spinal interneurons responsible for this pattern of activity.